Abstract
Psychosocial stress increases cardiovascular risk, which coincides with enhanced oxidative DNA damage. Increased sympathetic tone-related catecholamine release causes oxidative stress, which contributes to catecholamine-related cardiotoxicity. Therefore, we tested the hypothesis whether acute psychosocial stress induces oxidative DNA damage, its degree being related to the cardiovascular risk profile and depending on the sympathetic stress response. After assessment of the prospective cardiovascular Münster score (PROCAM) to determine the risk of acute myocardial infarction, 83 male and 12 female healthy volunteers underwent the Trier social stress test for groups (TSST-G). Heart rate variability was quantified by measuring the standard deviation (SDNN) and root mean square of successive differences (RMSSD) between normal-to-normal inter-beat intervals. Salivary α-amylase (sAA) activity was assessed as a surrogate for noradrenaline plasma concentrations. Oxidative DNA damage was determined using whole-blood single-cell gel electrophoresis (“tail moment” in the “comet assay”). A total of 33 subjects presented with a prospective risk of myocardial infarction (risk+) vs. 59 subjects without risk (risk-). The TSST-G stress significantly increased blood pressure, heart rate, and sAA in both groups, while oxidative DNA damage was only increased in the risk+ group. Immediately after the TSST-G, the “tail moment” showed significant inverse linear relations with both SDNN and RMSSD. Acute psychosocial stress may cause oxidative DNA damage, the degree of which is directly related to the individual cardiovascular risk profile and depends on the stress-induced increase in the sympathetic tone.
Highlights
Psychosocial stress is associated with cardiovascular risk [1,2], in part due to autonomic dysbalance resulting from a rise in sympathetic tone [3]
Our study tested the hypothesis that (i) acute psychosocial stress may cause oxidative DNA damage, (ii) the degree of which is directly related to the individual cardiovascular risk profile and (iii) depends on the stress-induced increase in the sympathetic tone
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Summary
Psychosocial stress is associated with cardiovascular risk [1,2], in part due to autonomic dysbalance resulting from a rise in sympathetic tone [3]. Increased superoxide radical formation contributes to catecholamine-related cardiotoxicity [4,5], and enhanced oxidative DNA damage coincides with cardiovascular risk [6]. Studies investigating the potential impact of social stress on oxidative stress-induced DNA damage are rare [7], and evidence of a putative association with sympathetic stress response is lacking. Our study tested the hypothesis that (i) acute psychosocial stress may cause oxidative DNA damage, (ii) the degree of which is directly related to the individual cardiovascular risk profile and (iii) depends on the stress-induced increase in the sympathetic tone
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